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Kazuhiro Ikenaka

Researcher at National Institutes of Natural Sciences, Japan

Publications -  305
Citations -  13182

Kazuhiro Ikenaka is an academic researcher from National Institutes of Natural Sciences, Japan. The author has contributed to research in topics: Oligodendrocyte & Myelin. The author has an hindex of 57, co-authored 295 publications receiving 12268 citations. Previous affiliations of Kazuhiro Ikenaka include Osaka University & Graduate University for Advanced Studies.

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The reeler gene-associated antigen on cajal-retzius neurons is a crucial molecule for laminar organization of cortical neurons

TL;DR: Findings revealed that the selective expression of a distinct molecule on Cajal-Retzius neurons is critical for the normal lamination of cortical neurons in the mammalian neocortex.
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The basic helix-loop-helix factor olig2 is essential for the development of motoneuron and oligodendrocyte lineages.

TL;DR: The data provide the first evidence that a single gene mutation leads to the loss of two cell types, motoneuron and oligodendrocyte, in the spinal cord of mice with a homozygous inactivation of Olig2.
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Molecular and Functional Characterization of a Novel Mouse Transient Receptor Potential Protein Homologue TRP7 Ca2+-PERMEABLE CATION CHANNEL THAT IS CONSTITUTIVELY ACTIVATED AND ENHANCED BY STIMULATION OF G PROTEIN-COUPLED RECEPTOR

TL;DR: These findings reveal an interesting correspondence of TRP7 to the background and receptor stimulation-induced cation currents in various native systems and suggest that the TRP6 channel is a new member of diacylglycerol-activated cation channels.
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Glutamate Transporter GLAST Is Expressed in the Radial Glia–Astrocyte Lineage of Developing Mouse Spinal Cord

TL;DR: The distinct changes in the cell position and morphology suggest that both the migration and transformation of radial glia cells begin in the spinal cord between E13 and E15, when the active stage of neuronal migration is over.
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Glial cell degeneration and hypomyelination caused by overexpression of myelin proteolipid protein gene.

TL;DR: Tight regulation of Plp gene expression is necessary for normal oligodendrocyte differentiation and survival, and its overexpression can be the cause of both dys- and demyelination.